Radiobiological damage to DNA of bacterial and mammalian cells can be repaired in vivo by two well-established pathways: excision repair pathway and a recA/exr mediated pathway. The recA/exr mediated, gap filling repair plays an important role in survival of cells after X-irradiation and UV irradiation. RecA/exr mediated repair is also considered an important part of the pathway originating with damaged DNA and ending with mutation. Alteration of recA/exr mediated repair with specific drugs, nutritional changes, and physical methods can markedly potentiate the effects of low dose radiation. The primary objective of this study is: (1) to analyze the degree of potentiation of UV and X-ray induced lethality in a genetically well-defined strain of Escherichia coli, (2) to measure the effects on forward mutation, (3) and to correlate different methods as to degree of potentiation with the type of physical-chemical alterations of the repair DNA intermediate. Effective potentiators of lethality but low mutation inductors originating from low intensity radiation would be determined. Classification as to the mode of repair alteration and correlation with successful potentiation of lethality will provide a criteria for further productive investigations. Control and understanding of low intensity radiation-induced damage potentiation through specific alteration of repair should provide explicit procedure for low intensity radiation therapy of cancer tissue.